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Anesth Analg 2008; 107:793-796 © 2008 International Anesthesia Research Society doi: 10.1213/ane.0b013e31818042d6
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Thoracic endovascular aortic reconstruction was contemplated but the traumatic aortic injury site lay directly opposite the ostium of the left subclavian artery and an arch-originating left vertebral artery and it was judged that optimal stent deployment could occlude these vessels and compromise the left common carotid artery (LCCA).1
The patient was taken to the operating room for hybrid arch replacement (Fig. 2). Hemodynamic monitoring included left radial artery catheter, an oximetric pulmonary artery catheter, and bifrontal rSO2 sensors (Invos Oximeter 5100C, Somanetics, Troy, MI). Anesthetics used included remifentanyl, pancuronium, and isoflurane gas.
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Surgery was performed via a median sternotomy with supra-aortic branch vessel translocation using the trimmed branched arch segment of a multi-branched polyester graft Gelweave Vascutek Plexus (Vascutek Ltd, Renfrewshire, UK) and a reversed saphenous vein graft between the graft and the left vertebral artery. The branched island of graft was anastomosed to the proximal ascending aorta (Fig. 2) using a partial occlusion clamp without cardiopulmonary bypass after administration of heparin 5000 IU IV. Hemostasis of this anastomosis was then secured and a reversed SV segment anastomosed to a proximal limb. Each supra-aortic vessel was then sequentially circumferentially mobilized, proximally ligated, distally clamped, anastomosed end-to-end to the graft limbs or SV and the reperfused in the sequence; innominate artery (IA-B) LCCA(C), left vertebral artery (SV-D) and left subclavian artery (E) (Letters as per Fig. 3). A 24 mm Medtronic Valiant stent graft (Medtronic Ltd, Hertfordshire, UK) was then deployed (Fig. 2) via the right femoral artery, stenting the aorta from native IA ostium to the proximal descending aorta excluding the traumatic aortic injury.1
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Figure 3 demonstrates the sequence of events, rSO2 values, SaO2, Pco2 and mean arterial blood pressure. Hemoglobin levels were maintained between 8 and 9 g/dL throughout the procedure. Baseline bilateral rSO2 approximated 75%. Application of the side biting clamp to the ascending aorta during a period of controlled hypotension to anastomose the crown of the multi-limbed graft to the ascending aorta, led to a differential decrease in the left and right rSO2 signals. After removal of partial occlusion clamp (A) the right rSO2 quickly returned to 60% whereas that of the left rSO2 recovered gradually, achieving equivalence prior to IA occlusion. During the IA anastomosis (B) there were modest (approximately 5%–8%) changes in the right and left rSO2 signals whereas during the LCCA anastomosis(C) there was a rapid decrease followed by gradual decline to 45% of the left rSO2 signal with recovery to 60% on reperfusion. The right rSO2 remained unchanged at 60%. The left vertebral artery anastomosis required retraction of the LCCA graft. As there was a rapid decline from 60% to 40% of the left rSO2 signal followed by gradual improvement to approximately 45% with maintenance of the right rSO2 at approximately 55%, we suspected retraction-based occlusion of the LCCA graft. Although we were reassured by the partial recovery of the left rSO2, during the left subclavian artery anastomosis (E), the left rSO2 again decreased to 40% recovering to only 50% on completion whereas the right rSO2 signal showed only a modest change.
Divergence of the signals continued and worsened during the stent deployment (F) with a deterioration of the left rSO2 to 45%. At the completion of the stent procedure, the LCCA graft was explored (G) and a partially occlusive thrombus removed. During this exploration there was minimal change in the right rSO2 and rapid decline after by a gradual improvement to 60%. As a discrepancy remained, following chest closure, the patient was immediately transferred for repeat CT scan which demonstrated satisfactory stent deployment but poor contrast enhancement of the LCCA with low flow detected on carotid duplex scanning. The patient was returned to the operating room where a repeat and complete thrombectomy was performed, unfortunately without rSO2 monitoring. Subsequent investigations during recovery indicated normal LCCA flow.
Postoperatively, the acute lung injury persisted and a tracheostomy was performed 14 days postoperatively. Agitation and reduced right-sided arm movement prompted a brain CT at day 19, which demonstrated a small left anterior hemorrhagic infarction in the middle cerebral artery territory. Subsequent clinical recovery was slow but uneventful and at 3 mo follow-up, the patient was fully ambulant and rehabilitated with a mild (4/5) right upper limb paresis.
DISCUSSION
Endovascular stent grafting is becoming the preferred treatment for traumatic aortic injury,2 particularly in the setting of multi-trauma when left thoracotomy, full heparinization, and cardiopulmonary bypass may be contraindicated. Supra-aortic vessel translocation is sometimes necessary to allow satisfactory proximal stent deployment to completely exclude the region of traumatic aortic injury. This case demonstrates the utility of NIRS and rSO2 assessment as an indicator of the adequacy of cerebral perfusion during such procedures.3
Although absolute values may not be accurately measured, decreasing rSO2 trends seem to reliably reflect decreasing cerebral hemoglobin oxygen saturation.4 We noted a 25%–30% actual decrease in the rSO2 signals during the arterial occlusions. The rSO2 signal represents the mean oxygen saturation of the venous and arterial compartments of the frontal lobe blood volume. As venous blood is 50%–60% saturated and comprises approximately 75% of the blood volume, the initial rSO2 signal of 75% suggests satisfactory cerebral oxygenation. The right-sided perturbations in rSO2 were short-lived and recoverable, whereas the divergence and continuing decline of the left signal was assumed to indicate compromised oxygen delivery and prompted re-exploration of the LCCA graft. Incomplete recovery after thrombectomy prompted further investigation and a further definitive thrombectomy. Although additional intraoperative investigations, including carotid duplex, angiography, and transcranial Doppler assessment of middle cerebral artery flow, may have been helpful, these were not available in this case. We believe a failure to monitor and detect these rSO2 changes may have led to a catastrophic cerebral event. The rSO2 signal shows a biphasic decline when arterial perfusion is interrupted with an initial rapid decrease followed by a gradual decline. During carotid endarterectomy a decrease in rSO2 signals to <55% is associated with neurological compromise.5
A decrease in rSO2 may also occur due to factors other than reduced arterial blood flow, including reduced arterial oxygen saturation, severe anemia, increased brain oxygen consumption, and venous congestion. In our case, hemoglobin levels and arterial SaO2 were maintained (using an increased Fio2 and alveolar recruitment maneuvers). Although the innominate vein was maintained intact during the reconstruction, transient vein occlusion during retraction may have contributed to the per-anastomotic rSO2 changes but were unlikely to have induced the continued divergence of right and left rSO2 signals. In addition, the patient had a slightly high arterial Pco2 due to his acute lung injury. Thus, the cause of rSO2 change appeared predominantly attributable to arterial occlusions. However, the signal divergence during proximal anastomosis of the graft crown is difficult to explain, and although this resolved, it remains possible that there was a pre-existing embarrassment of the left frontal circulation that enhanced the subsequent changes.
There are some limitations of NIRS monitoring for cerebral ischemia. Embolic infarction in non-monitored sites may occur without signal change and thus a maintained signal is not an assurance of cerebral well being. Electrocautery may also interfere with NIRS monitoring but is used mostly during sternal entry and closure and not during the aortic reconstruction. Moreover NIRS is not capable of differentiating the cause of the rSO2 change. However, such monitoring can provide a warning that cerebral ischemia is likely to be present at a given moment. Once cerebral ischemia is suspected from the NIRS data, further investigations may clarify the cause.6
The use of NIRS in cardiac surgery is currently sporadic, although recent evidence suggests that such monitoring may improve outcomes and guide cardiopulmonary bypass management.7,8 In the scenario of hybrid arch reconstruction, this case strongly suggests NIRS can be a very important real-time monitoring tool in such procedures.
Footnotes
Accepted for publication May 1, 2008.
Reprints will not be available from the author.
REFERENCES
- Kwolek CJ, Fairman R. Update on thoracic endovascular grafting using the medtronic talent device. Semin Vasc Surg 2006;19:25–31[Web of Science][Medline]
- Criado FJ, Barnatan MF, Rizk Y, Clark NS, Wang CF. Technical strategies to expand stent-graft applicability in the aortic arch and proximal ascending aortic dissection. J Endovasc Ther 2002;9:32–8[Web of Science]
- Bhatia R, Hampton T, Malde S, Kandala NB, Muammar M, Deasy N, Strong A. The application of near-infrared oximetry during aneurysm embolization: a comparison with intraprocedural angiography. J Neurosurg Anesthesiol 2007;19:97–104[Web of Science][Medline]
- Janelle GM, Mnookin S, Gravenstein N, Martin T, Urdaneta F. Unilateral cerebral oxygen desaturation during emergent repair of a DeBakey type 1 aortic dissection: potential aversion of a major catastrophe. Anesthesiology 2002;96:1263–5[Web of Science][Medline]
- Hirofumi O, Otone E, Hiroshi I, Satosi I, Shigeo I, Yasuhiro N, Masato S. The effectiveness of regional cerebral oxygen saturation monitoring using near-infrared spectroscopy in carotid endarterectomy. J Clin Neurosci 2003;10:79–83[Web of Science][Medline]
- Orihashi K, Sueda T, Okada K, Imai K. Near–infrared spectroscopy for monitoring cerebral ischemia during selective cerebral perfusion. Eur J Cardiothorac Surg 2004;26:907–11
[Abstract/Free Full Text] - Murkin JM, Adams SJ, Novick RJ, Quantz M, Bainbridge D, Iglesias J, Cleland A, Schaefer B, Irwin B, Fox S. Monitoring brain oxygen saturation during coronary bypass surgery: a randomized prospective study. Anesth Analg 2007;104:51–8
[Abstract/Free Full Text] - Edmonds HL Jr, Rodriguez RA, Audenaert SM, Austin III EH, Pollock SB Jr, Ganzel BL. The role of neuromonitoring in cardiovascular surgery. J Cardiothoracic Vasc Anesth 1996;10:15–23[Web of Science][Medline]
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